Volatile Substance Abuse: Demographic Patterns, Clinical Toxicology,and Emergency Management
Authors: Earl J. Reisdorff, MD, FACEP, Program Director, Michigan State University Emergency Medicine ResidencyLansing, Michigan Capital Medical Center and Sparrow Hospital, Lansing, MI.
Mary Beth Miller, DO, Assistant Director-Education, Michigan State University Emergency Medicine ResidencyLansing, Michigan Capital Medical Center and Sparrow Hospital, Lansing, MI.
Although volatile substance abuse (VSA) with toluene, aromatic hydrocarbons, or butane does not make the same splashy headlines as the recreational abuse of cocaine, marijuana, or heroin, the problems associated with solvent inhalation are potentially destructive and must be recognized by the emergency practitioner. (See Table 1.)
Although most abusers of solvent substances never access the ED for medical attention, severe cases of volatile substance abuse can produce ventricular fibrillation, asphyxiation, noncardiogenic pulmonary edema, and various neuropsychiatric syndromes. Considering that volatile substances capable of producing euphoria and intoxication are so ubiquitous that they can be found in such common household products as glue, typewriter correction fluid, and cigarette lighters, it is not surprising that up to 20% of American high school students have reported experimentation with these types of "recreational" substances.1
This review presents a clinically useful outline of the demographic patterns associated with VSA as well as a substance-by-substance discussion of the clinical manifestations and toxicological consequences of acute and chronic abuse. A detailed discussion of the presenting signs and symptoms as well as the potential life-threatening cardiac complications associated with solvent inhalation will prepare the ED physician to treat patients who present with volatile substance abuse syndromes.
Solvents are volatile hydrocarbons that evaporate rapidly at room temperature. These chemicals are absorbed into the blood through the lungs. Because solvents are extremely lipid soluble, they rapidly enter organs with a high fat content, including the brain. Metabolism and excretion are determined by the type of agent inhaled. Most agents are excreted directly through the lungs, although isolated substances are excreted in the urine after hepatic metabolism. For example, methylene chloride is metabolized in the liver, producing carbon monoxide. Carbon monoxide binds avidly to hemoglobin and is slowly excreted during respiration. Some inhalants, such as freons, leave the body through respiration essentially unchanged.
The abuse of inhaled solvents is most appropriately called volatile substance abuse (VSA). It should be stressed that many other drugs of abuse, including marijuana, cocaine, and methamphetamine, are also inhaled for their stimulatory effects. Even fentanyl patches have been heated and the vapors inhaled for illicit purposes. These drugs, however, are not solvents, and therefore do not share the same chemical and physical properties of commonly abused inhalant agents.
From a clinical perspective, VSA involves solvents that readily vaporize at room temperature. Because inhalants are inexpensive, readily found in the home, and can be legally purchased by people of all ages in some states, the potential for VSA is significant. With the exception of the nitrite group (e.g., amyl nitrite), abused inhalants have potent psychoactive properties.
Commonly abused agents include typewriter correction fluid (trichloroethane), gasoline, toluene, nitrites, and acetone (nail polish remover). In addition, such ordinary household products as all-purpose cleaning fluids, acrylic spray paints, paint thinners, model glue, and aerosol propellants (e.g., hair spray, room deodorizers, insecticides, and deodorants) also have abuse potential. Other agents that are frequently used for inducing psychoactive effects include "magic" marker and highlighter pens, lighter fluid, and antifreeze. Among Native American youths, gasoline is a commonly inhaled abuse agent. 2
Demographic Patterns. From a recreational perspective, solvents are inhaled for their inebriating effects, which range from lightheadedness and euphoria to disorientation and frank intoxication. The use of solvents as euphoria-inducing agents became widespread in the 1960s. In this regard, VSA became entrenched as a recreational pursuit in California with the advent of gasoline sniffing.2 Soon thereafter, glue sniffing emerged as a common practice among adolescents, a practice that became widely reported in the United States and Great Britain.3,4
Although VSA extends into all demographic groups, it is most prevalent among urban adolescents of lower socioeconomic levels, especially among those individuals who have poor school performance.3,4 Among adolescents in Mexico, there is a specific association between inhalant abuse and juvenile delinquency, with some studies reporting that 23% of Mexican juvenile offenders have used inhalants.5 In fact, among eighth graders in certain geographic areas, VSA is more common than smoking marijuana. Not surprisingly, patterns of abuse are characterized by specific features. For example, VSA is frequently carried out in groups, primarily among adolescent boys.6 In this setting, abuse of multiple agents is a common practice. A number of volatile substances may be passed around, or an inhalant may be used in combination with other drugs such as marijuana or alcohol.
Generally, VSA tends to be limited to brief periods of experimentation. However, some abusers continue this destructive practice well into adulthood, sometimes abusing a series of different drugs. There is a tendency for users to migrate from abuse of solvents to chronic ethanol abuse.7 In fact, some studies suggest that inhalant abuse may be an independent risk factor for intravenous (IV) drug use. Even when adjusting for sex, age, race, socioeconomic status, and marijuana use, inhalant users were still 5.3 times more likely than nonusers to have injected drugs.8
Unfortunately, the prevalence of VSA is very difficult to quantitate, as are the actual number of deaths from the intentional inhalation of solvents. In England, however, the mortality rate from VSA appears to be increasing.9 Between 1970 and 1991, 91 deaths were reported in Great Britain. During the period 1991 to 1993, 185 deaths were reported. Among these fatalities, 51% were caused by direct toxic effects from the inhalant. In addition, 21% of deaths were associated with asphyxia, 18% with aspiration, and 11% were caused by trauma-related circumstances (e.g., drowning, autoerotic strangulation).
Morbidity and Mortality Features. In the United States, the majority of deaths linked to VSA have been reported in males 15-19 years old.10 Fuel gases (butane, propane, gasoline), trichloroethane (typewriter correction fluid, dry cleaning fluids), and freons (especially bromochromodifluoromethane found in yellow fire extinguishers) are responsible for 60% of these deaths.10 Deaths can also occur from the unintentional inhalation of these agents, such as when a fire extinguisher is discharged inside of a battle tank.11 Habitual abusers generally prefer toluene-based solvents for the high degree of euphoria that they allegedly produce. Another agent commonly found among abusers is gold acrylic spray paint. Gold acrylic spray paint is alleged to produce unique psychoactive effects not found in other colors of paint. Typewriter correction fluid (trichloroethane) is a popular substance of abuse among adolescents.
The National Institute of Drug Abuse’s annual survey of high school graduates suggests a lifetime incidence of about 15-20%.1 Although one British report suggests that as many as 13% of adolescents routinely abuse inhalants, a more recent study from England suggests that 3.5-10% of current adolescents have at least experimented with solvents.12,13 One U.S. survey of 10,198 middle school and high school students showed a lifetime volatile substance usage rate of 12.8%, with 4.8% of students reporting they had used inhalants for a euphoric effect in the previous month. Interestingly, inhalant use increases during grades 6-8 and begins to decline in grades 10-12.14 Since 1988, inhalant use has become more common than marijuana use among eighth graders.15 Of all calls made to a regional poison center that originate in schools, 7% involve inhalant-related questions or problems.16
Attempts to curb VSA have met with variable success. Warning labels that indicate what materials are inhalants may actually serve to draw the abuser’s attention to the product.17 Some manufacturers have added mucosal irritants such as oil of mustard to deter abuse.
Abuse of solvents occurs through three primary activities: sniffing, bagging, and huffing. Sniffing is the act of inhaling the solvent directly from an open container such as a can or jar. Gasoline is commonly abused in this manner. The bagging technique requires the solvent to be poured or sprayed into a bag (e.g., a potato chip bag). The bag is then placed over the mouth and nose and the person breathes deeply. Solvent vaporization is enhanced by shaking the plastic bag. As might be expected, bagging is the most dangerous method of inhalation, because increased solvent levels are achieved and hypoxia is more likely. Complications include suffocation, which can occur if the bag adheres to the face of a lethargic patient. Another danger is aspiration, which results if the person vomits into the bag. Despite these hazards, bagging is the preferred method of abuse since the highest amount of solvent vaporization is achieved. Huffing is the practice of inhaling vapors by placing a solvent-soaked cloth (e.g., a rag or sock) over the mouth and nose. One variant of huffing involves breathing fumes from solvent-soaked cotton balls that are placed in the reservoir of a dust protection mask or gas mask. This is particularly dangerous because of the high risk of hypoxia as well as vomiting and aspiration.
Overview. The toxicological and clinical effects of volatile substances are variable. The majority of inhalants can produce neurologic dysfunction, asphyxia, and cardiovascular abnormalities that range from rhythm disturbances to myocardial suppression. Typically, abusers can be expected to develop some degree of inebriation, ranging from mild euphoria to frank psychosis. Other clinical signs and symptoms include blurred vision, photophobia, tinnitus, slurred speech, headache, conjunctival injection, and abdominal pain. Transient hypertension, salivation, persistent sneezing and coughing, chest pain, and bronchospasm have also been described.
Cardiac arrhythmia is the primary cause of death from VSA. Other contributing mechanisms include myocardial sensitization to catecholamines, hypoxemia, respiratory depression, vagal stimulation, aspiration, laryngospasm (especially with butane inhalation), and associated trauma (e.g., drowning).10
Neurologic Manifestations. The primary effect of abused inhalants is central nervous system (CNS) depression. Predictably, an inebriated or intoxicated state is produced that is similar to that seen with ethanol or marijuana use. Initially, there is a state of euphoria that is quickly followed by progressive CNS depression. Other reported effects include excitement, tinnitus, slurred speech, bizarre behavior, syncope, and seizures. Visual and auditory hallucinations have been reported with gasoline, lighter fluid, and toluene use.
It is postulated that the euphoria accompanying VSA provides the psychological reinforcement that leads to long-term abuse. Whether or not VSA leads to physical addiction is unclear. Generally speaking, however, physical dependence characterized by a physical withdrawal syndrome has not been described for most volatile substances. One exception is toluene habituation, a syndrome in which sudden cessation of the solvent can produce a syndrome similar to that encountered with alcohol withdrawal. A similar withdrawal syndrome has been suggested for butane abuse.18
Patients suffering the acute effects of volatile substances usually appear drunk; consciousness is almost always clouded in moderate to severe inhalations. Typically, a state of inebriation occurs within a few seconds of inhalation. Hypoxia and hypercapnia, which result from bagging, accentuate the CNS depressive effects. Intoxication lasts from 10 minutes to three hours depending on the type of agent, the exposure concentration, the duration of exposure, and the rate of detoxification (metabolism) by the patient. It is possible to induce general anesthesia in humans with toluene after one minute of steady inhalation with high concentrations attained while bagging.
Long-term CNS effects related to solvent abuseparticularly in individuals with chronic toluene inhalationinclude encephalopathy, cerebellar degeneration, and disorders of equilibrium.19,20 Irreversible structural changes may also occur. For example, the neuropathologic effect in people who chronically sniff paint, so-called "spray heads," is neuronal demyelination. Because of their chemical properties, many solvents also have the capacity for "liquefying" fat. Because the brain is a lipid-rich organ, chronic solvent abuse essentially "dissolves" brain cells. This appears as brain atrophy and discoloration of cerebral and cerebellar white matter. Microscopic analysis reveals unique oval membrane-bound cytoplasmic bodies filled with inclusions.21
On neuroimaging studies, the manifestations of chronic paint sniffing appear as a loss of cerebral and cerebellar gray-white matter discrimination, scattered multifocal deep white-matter lesions, and gross generalized atrophy of the cerebrum, cerebellum, and the corpus callosum.22 Specifically, MRI findings in chronic toluene abusers include abnormalities in the middle cerebellar peduncle and the cerebellar white matter. Lesions also are observed in the deep cerebral white matter, the posterior limb of the internal capsule, thalamus, and basal ganglia.23
In addition, VSA can produce a syndrome similar to Parkinson’s disease. This complication occurs most often with lacquer thinner.24 The symptoms can be indistinguishable for idiopathic parkinsonism (Parkinson’s disease). Clinical findings may persist for months and, in some cases, respond to levodopa therapy.24 Cerebral infarction and hemiplegia also have occurred as a result of vasospasm associated with VSA.25 Peripheral neuropathies, such as those seen with hexane, can also occur.26
Other findings encountered in chronic inhalant abusers (particularly those who abuse toluene) include persistent paranoid psychosis and, perhaps, an increased risk of temporal lobe epilepsy.27 In particular, ototoxicity has been associated with toluene.28 Finally, poor school performance and behavioral disorders are associated with VSA. However, it is argued that many of the neuropsychiatric disturbances associated with VSA result from social disadvantages and a history of delinquency. When controlled for these variables, neuropsychiatric sequelae may not be a direct result of substance abuse.29
Pulmonary Complications. All solvents are simple asphyxiants. The vapor displaces oxygen from the alveoli and, in the process, decreases the amount of oxygen that is available to pass across the alveolar membrane and into the blood. In addition, the various practices by which solvents are inhaled (especially bagging) can exacerbate hypoxia. The hypoxic effect, by itself, is sufficient to cause death.30
Other pulmonary effects result primarily from direct alveolar damage. In this regard, inhalation of high concentrations of hydrocarbon vaporsespecially toxic hydrocarbonscan produce severe chemical pneumonitis. Alveolar membrane damage can cause cardiogenic pulmonary edema, further exacerbating hypoxemia. In some cases, VSA can cause acute eosinophilic pneumonia. The clinical presentation is identical to idiopathic acute eosinophilic pneumonia and may require mechanical ventilation.31
Cardiovascular Effects. Cardiac arrhythmia is the most common cause of sudden, VSA-related mortality. Although the exact mechanism by which volatile abused substances produce arrhythmias is unclear, sensitization of the myocardium to endogenous catecholamines is a likely cause. Other factors that may have a role in the genesis of cardiac arrhythmias include electrolyte imbalances, hypoxia, acidosis, coronary artery spasm, and myocardial infarction.
A bizarre and, unfortunately, fatal phenomenon associated with VSA is called sudden sniffing death. In these cases, the affected individual typically acts startled, jumps up, runs about, and then collapses in ventricular fibrillation. This syndrome occurs without a subjective prodrome, giving the abuser no warning that death may occur. As a result, the substance abuser is unable to detect warning signs that might caution him or her to stop before the fatal event ensues. In Great Britain, sudden sniffing death syndrome is responsible for 55% of the deaths associated with VSA.32 As an explanation for sudden sniffing death, it is theorized that the inhalants sensitize the myocardium to endogenous epinephrine. When the level of circulating epinephrine suddenly increases, such as when one is startled, the irritable myocardium fibrillates. The exact mechanism by which this occurs remains unknown.
Among commonly abused volatile substances, fluorinated hydrocarbons (freons) are commonly implicated as a cause of arrhythmias associated with VSA. Bretylium may have a theoretical advantage over other antiarrhythmics for treating ventricular fibrillation. Of the halogenated hydrocarbons, trichloroethane (typewriter correction fluid) is also known to precipitate fatal cardiac dysrhythmias. Acute myocardial infarction has occurred from coronary vasospasm caused by toluene sniffing. Finally, glue sniffer’s heart, a dilated cardiomyopathy, can result from chronic VSA.
Miscellaneous Effects. Long-term toxic sequelae caused by VSA involve almost every organ system. Primary sites of injury include the liver, kidneys, central and peripheral nervous systems, and bone marrow. (See Table 2.) With respect to neuropsychiatric symptoms, chronic inhalant abuse can cause anorexia, listlessness, and extreme moodiness. Although somewhat rare, acute tubular necrosis, renal failure, glomerulonephritis, and nephrotic syndrome can also occur. The renal insult may result in permanent renal dysfunction.
Hepatic damage also occurs, especially in the setting of toluene, trichloroethylene, chloroform, and carbon tetrachloride abuse. Bone marrow depression, aplastic anemia, and leukemia are associated with sniffing certain glues,33 whereas lead poisoning can develop from inhaling leaded gasoline. This is more common on Native American reservations where leaded gasoline is still widely available. Patients abusing acetone can present in a fashion similar to diabetic ketoacidosis; in these patients, however, the ketonemia is more pronounced than the acidosis.
Glue-Sniffing (Toluene). Generally speaking, only glues containing aromatic hydrocarbons (e.g., toluene) have the potential for abuse. As far as availability, toluene is found in household plastics, model cement, and lacquer thinner. It is an extremely potent neurotoxin and can produce a peripheral, sensorimotor neuropathy with a stocking-glove distribution. This is especially likely to occur when N-hexane is combined with toluene. Muscle weakness of the lower extremities has also occurred after sniffing pure toluene.34 The dramatic clinical presentation of motor weakness associated with VSA can be confused with Guillain-Barré syndrome.35
Chronic toluene abuse can lead to permanent cerebellar ataxia, chronic encephalopathy, headaches, and personality changes. Toluene abuse during pregnancy has been implicated in intrauterine growth retardation, premature delivery, and congenital malformations (renal and skeletal).36 Renal abnormalities linked to glue sniffing include nephrotic syndrome, nephritis, and renal tubular acidosis. Adult glue sniffers commonly present with neuropsychiatric disorders, gastrointestinal disorders, or muscle weakness. Toluene can also cause a hyperchloremia and acidosis accompanied by impaired urinary acidification.34 The anion gap may be normal or elevated. Hypokalemia can be severe and contribute to both weakness and arrhythmias. Though some effects may be transitory, proximal and distal tubular dysfunction may persist.34
Gasoline. Gasoline abuse is frequently seen among the displaced native peoples in the United States, Canada, Mexico, South Africa, and Australia.37 Gasoline is a complex mixture of hydrocarbons, some of which have powerful narcotic-like properties. Other unsaturated hydrocarbons contained in gasoline have anesthetic properties and can cause nausea, ataxia, and coma. While inhaling gasoline, the abuser may experience intense excitement followed by coma. Profound intoxication can cause marked respiratory depression and cardiac irritability that can be fatal.38
Abuse of gasoline usually involves inhalation directly from a can or glass jar. Intoxication occurs after 10-20 breaths and lasts for 3-5 hours. Intoxication is frequently accompanied by nausea and vomiting, which increases the risk of aspiration during the inebriated state. Where "leaded" gas is still available, lead toxicity can occur. The primary additive is tetraethyl lead. Tetraethyl lead and its metabolites are extremely neurotoxic and can produce a syndrome of ataxia, tremor, and encephalopathy in chronic users.39,40
Butane. Butane is the major flammable ingredient of cigarette lighter refills, camping stoves, and small blowtorches. It is commonly mixed with propane and can cause toxicity as a result of simple asphyxiation. The gas from cigarette lighter refills is released by using the teeth to press the nozzle. This practice can easily cause a fire, resulting in orofacial burns and laryngoedema.
Halogenated Hydrocarbons. Halogenated hydrocarbons include chlorinated as well as fluorinated hydrocarbons (freons). Chlorinated hydrocarbons include carbon tetrachloride, trichloroethane , and trichloroethylene. These agents initially cause euphoria and a sense of excitement that is promptly followed by headache, dizziness, nausea, and vomiting. Intoxication can eventually lead to stupor, coma, and seizures. Typewriter correction fluid, which contains 52% trichloroethane, is one of the most commonly abused substances among teenagers. Of special concern is the fact that chlorinated hydrocarbons cause acute renal failure and hepatic necrosis. Since the hepatic damage is centrilobular, N-acetylcysteine (Mucomyst) has been suggested as a possible treatment modality. Its effectiveness in this setting, however, is unproven. Trichloroethylene causes optic nerve atrophy and cranial nerve damage.
Freons, which are responsible for an alarming number of VSA-related deaths, can produce ventricular dysrhythmias including ventricular fibrillation. Freons have been used extensively as propellants and in cooling systems such as refrigerators and air-conditioning units. They are also used in yellow fire extinguishers and in some upholstery protection agents. In one reported case, a 15-year-old boy developed ventricular fibrillation after intentionally inhaling freon from an automobile air conditioner recharge unit. Cardiopulmonary resuscitation was started, and, after administering bretylium, a sinus tachycardia resulted; neurologic recovery was complete.41
Methylene Chloride. Methylene chloride, which has been associated with a unique constellation of problems, is commonly found in paint thinners and is metabolized by the liver to carbon monoxide. Although the primary toxic effects result directly from the agent, the amount of carbon monoxide produced is significant and can adversely affect an already compromised patient.42 As opposed to exposure by direct inhalation, carbon monoxide is produced even after removal from the source of exposure and has a half-life 2.5 times that of inhaled carbon monoxide at room air.43 The toxic effects of carbon monoxide, such as hemoglobin binding, myoglobin binding (including cardiac myoglobin), and suppression of mitochondrial respiration, can further exacerbate the effect of the parent compound.
Nitrous Oxide. Nitrous oxide was first used as an inhalational anesthetic and is still used as an anesthetic-analgesic. It is used commercially in the cartridges for whipped cream dispensers. Referred to as whippets among the drug culture, these can be obtained legally. Whippets are used for their mild intoxicating effects. The primary clinical concern associated with nitrous oxide is its propensity for causing fatal hypoxia. Chronic abuse may cause demyelination and neuropathy.
Nitrites. Although nitrites are commonly abused inhalants, they are neither solvents nor are they psychoactive agents. Their primary effects are cardiovascular (vasodilation). In fact, since 1867, amyl nitrite had been used medicinally to relieve angina pectoris. Slang terms for nitrites are bullet, hardware, lightning bolt, locker room, rush, sweat, and thrust. Amyl nitrite pearls are found in cyanide treatment kits and are called poppers or snappers. Amyl nitrite is available in cotton-wrapped ampules designed to be crushed, and then inhaled. Patients describe feeling light-headed and having a throbbing, vascular, migraine-like headache.
Nitrites can cause methemoglobinemia, cyanosis, and hypotension. Though the methemoglobinemia usually results from ingestion of amyl, butyl, or isobutyl nitrites, inhalation of amyl nitrite can cause symptomatic methemoglobin levels.44 Fatal methemoglobinemia from inhalation of isobutyl nitrite has also been reported.45 Methemoglobinemia is managed by administering methylene blue in an initial dose of 2 mg/kg IV push over 3-5 minutes. Inhaling volatile nitrites has also caused hemolytic anemia.46
Nitrites are frequently abused by homosexual men, who use the drug for its alleged aphrodisiac effects. The drug reportedly causes relaxation in the anal sphincter. Amyl nitrite does cause some smooth muscle relaxation. Some studies suggest a tenuous association between the HIV virus and nitrite abuse in the clinical expression of AIDS. Clearly, however, abuse of nitrite inhalants has been epidemiologically associated with Kaposi’s sarcoma.47 Transient, reversible hematologic and immune suppression are seen with inhalational exposure to isobutyl nitrite.48,49
There are no clear identifying features of VSA, nor does the clinical presentation follow any distinct toxidrome pattern. In the ED, the patient appears inebriated. The odor of gasoline or solvents on the hair, breath, or clothing may suggest the diagnosis. Because many solvents are excreted through the lungs, the odor of solvents is strongest on the breath, where it may be detected for hours.50
On physical examination, the midface may be marked with an acrylic paint, typewriter correction fluid, or glue. An erythematous rash may be present around the mouth as a result of repetitive inhalation. This is commonly referred to as glue sniffer’s rash. EMS personnel, family, or friends may report empty adhesive tubes, aerosol spray cans, cigarette lighter refills, or potato chip bags at the scene.51 Patients may present with thermal burns, denying that an errant episode of solvent abuse led to the injury.
If the aforementioned clinical clues are lacking, a thorough, systematic search to uncover the etiology of the patient’s altered mental status must be initiated. Metabolic, infectious, traumatic, or drug-induced causes should be excluded.
The primary treatment for inhaled solvents focuses on eliminating the offending toxin and treating the acute symptoms. (See Table 3.) The airway, breathing, and circulation must be evaluated and stabilized as necessary. The majority of people recover rapidly from VSA intoxication and, therefore, never seek medical consultation. Most cases are adequately treated by simply removing the inhalant and providing oxygen. However, endotracheal intubation and mechanical ventilation may be required in the comatose patient.
Because myocardial irritability can be a problem, great caution should be used when considering the use of epinephrine and other catecholamines. If the patient already presents in ventricular fibrillation, standard ACLS protocols should be initiated. Successful suppression of ventricular dysrhythmiaalbeit anecdotalhas been reported using phenytoin as an antiarrhythmic.52 Brady proposes a theoretical advantage to bretylium as an agent to treat freon-induced ventricular fibrillation.41 The adrenergic (ganglionic) blocking effect as well as the antiarrhythmic effect of bretylium may present an advantage over Class 1 antiarrhythmics.
Burns have been reported more frequently with butane cigarette lighter fluid abuse. They tend to be fairly minor, with an average hospital stay of two days, but may be particularly severe if the patient is stuporous at the time the fire begins.53,54 Any thermal burns should be treated in the standard manner.
If the patient has had extended loss of consciousness and has been lying on the floor, rhabdomyolysis may be present.41 The diagnosis is made by obtaining a serum myoglobin level and urinalysis for myoglobinuria. Tea-colored urine or a urinalysis with chemical markers suggesting a large amount of blood yet few red blood cells on microscopic examination suggests rhabdomyolysis.
Profound metabolic acidosis and severe electrolyte disturbances may be life-threatening. An arterial blood gas should be performed to determine the degree of hypoxia; a carboxyhemoglobin level should be obtained, and the presence of methemoglobin should be evaluated. In the hypoxic patient, or in the patient with abnormal auscultatory findings, a chest radiograph should be performed to exclude noncardiogenic pulmonary edema.
Carboxyhemoglobin is treated with oxygen and methemoglobin with methylene blue. The emergency physician may consider a more comprehensive evaluation of the patient to detect long-term pathophysiologic effects by assessing a complete blood count, urinalysis, electrolytes, blood urea nitrogen (BUN), creatinine, and liver function studies. The blood count helps determine hematologic toxicity; the urinalysis, BUN, and creatinine assess renal impairment; electrolytes are essential for measuring an anion gap acidosis; and the liver studies define any hepatotoxicity. Routine urine and serum drug screens do not detect these substances of abuse. Levels of salicylate and toxic alcohols should be considered if the diagnosis is unclear.
Volatile substance abuse has become a serious health concern, especially among young adolescents. Inhalants are easily obtained. Both immediate and long-term effects are associated with considerable morbidity and, in some cases, can cause death. Emergency physicians should consider VSA and its complications in patients who present to the ED in an inebriated state.
1. Johnston LD, O’Malley PM, Bachman JG. Prevalence of drug user among 8th, 10th, and 12th grade students. In: National Survey Results on Drug Use from Monitoring the Future Study, 1975-1992. Rockville, MD: National Institute on Drug Abuse-U.S. Dept of Health and Human Services; 1993.
2. Bass M. Sudden sniffing death. JAMA 1970;212:2075-2079.
3. Glaser HH, Massengale ON. Glue sniffing in children: Deliberate inhalation of vaporized plastic cements. JAMA 1962;181:300-303.
4. Merry J, Zachariadis N. Addiction to glue sniffing. BM J 1962;2:1448.
5. Tapia-Conyer R, Cravioto P, De La Rosa B, et al. Risk factors for inhalant abuse in juvenile offenders: The case of Mexico. Addiction 1995;90:43-49.
6. Masterton G, Sclare AB. Solvent abuse. Health Bull (Edinb) 1978;36:305-309.
7. Cohen S. Glue sniffing. JAMA 1975;231:653-654.
8. Schutz CG, Chilcoat HD, Anthony JC. The association between sniffing inhalants and injecting drugs. Compr Psychiatry 1994;35:99-105.
9. Anderson HR, Macnair RS, Ramsey JD. Deaths from abuse of volatile substances: A national epidemiologic study. BM J 1985;290:304-307.
10. Adgey AA, Johnston PW, McMechan S. Sudden cardiac death and substance abuse. Resuscitation 1995;29:219-221.
11. Lerman Y, Winkler E, Tirosh MS, et al. Fatal accidental inhalation of bromochlorodifluoromethane (Halon 1211). Hum Exp Toxicol 1991;10:125-128.
12. Gay M, Meller R, Stanley S. Drug abuse monitoring: a survey of solvent abuse in the county of Avon. Hum Toxicol 1982;1:257-263.
13. Langa A. Volatile substance abuse: A brief report. Br J Clin Pract 1993;47:94-96.
14. Hansen WB, Rose LA. Recreational use of inhalant drugs by adolescents: A challenge for family physicians. Fam Med 1995;27:383-387.
15. Edwards RW. Drug use among 8th grade students is increasing. Int J Addict 1993;28:1613-1620.
16. Perry PA, Dean BS, Krenzelok EP. A regional poison center’s experience with poisoning exposures occurring in schools. Vet Hum Toxicol 1992;34:148-151.
17. Liss BI. Government, trade, and industry and other preventative responses to volatile substance abuse. Hum Toxicol 1989;8:327-330.
18. Evans AC, Raistrick D. Phenomenology of intoxication with toluene-based adhesives and butane gas. Br J Psychiatry 1987;150:769-773.
19. Knox JW, Nelson JR. Permanent encephalopathy from toluene inhalation. N Engl J Med 1966;275:1494-1496.
20. Sera M, Igarashi S, Miyazaki T, et al. Equilibrium disorders with diffuse brain atrophy in long-term toluene sniffing. Arch Otorhinolaryngol 1978;221:163-169.
21. Kornfeld M, Moser AB, Moser HW, et al. Solvent vapor abuse leukoencephalopathy: Comparison to adrenoleukodystrophy. J Neuropathol Exp Neurol 1994;53:389-398.
22. Xiong L, Matthes JD, Li J, et al. MR imaging of "spray heads": Toluene abuse via aerosol paint inhalation. AJNR Am J Neuroradiol 1993;14:1195-1199.
23. Kojima S, Hirayama K, Furumoto H, et al. Magnetic resonance imaging in chronic toluene abuse and volitional hyperkinesia. Rinsho Shinkeigaku 1993;33:477-482.
24. Uitti RJ, Snow BJ, Shinotoh H, et al. Parkinsonism induced by solvent abuse. Ann Neurol 1994;35:616-619.
25. Prendergrast MC. Hydrocarbons and inhalants. In: Reisdorff EJ, Roberts MR, Wiegenstein JG, eds. Pediatric Emergency Medicine Philadelphia: WB Saunders; 1993:712.
26. Byrne A, Kirby B, Zibin T, et al. Psychiatric and neurological effects of chronic solvent abuse. Can J Psychiatry 1991;36:735-738.
27. Tenenbein M, DeGroot W, Rajani KR. Peripheral neuropathy following intentional inhalation of naphtha fumes. Can Med Assoc J 1984;131:1077-1079.
28. Pryor GT, Rebert CS, Dickinson J, et al. Factors affecting toluene-induced ototoxicity in rats. Neurobehav Toxicol Teratol 1984;6:223-238.
29. Chadwick OF, Anderson HR. Neuropsychological consequences of volatile substance abuse: A review. Hum Toxicol 1989;8:307-312.
30. Winek CL, Wahba WW, Rozin L. Accidental death by nitrous oxide inhalation. Forensic Sci Int 1995;73:139-141.
31. Kelly KJ, Ruffing R. Acute eosinophilic pneumonia following intentional inhalation of Scotchguard. Ann Allergy 1993;71:358-361.
32. Ramsey J, Anderson HR, Bloor K, et al. An introduction to the practice, prevalence and chemical toxicology of volatile substance abuse. Hum Toxicol 1989;8:261-269.
33. Powars D. Aplastic anemia secondary to glue sniffing. N Engl J Med 1965;273:700-702.
34. Kamijima M, Nakazawa Y, Yamakawa M, et al. Metabolic acidosis and renal tubular injury due to pure toluene inhalation. Arch Environ Health 1994;49:410-413.
35. Streicher HZ, Gabow PA, Moss AH. Syndromes of toluene sniffing in adults. Ann Intern Med 1981;94:758-762.
36. Donald JM, Hooper K, Hopenhayn-Rich C. Reproductive and developmental toxicity of toluene: A review. Environ Health Perspect 1991;94:237-244.
37. Chalmers EM. Volatile substance abuse. Med J Aust 1991;154:269-274.
38. Poklis A, Burkett CD. Gasoline sniffing: A review. Clin Toxicol 1977;11:35-41.
39. Valpey R, Sumi SM, Copass MK, et al. Acute and chronic progressive encephalopathy due to gasoline sniffing. Neurology 1978; 28:507-510.
40. Ross CA. Gasoline sniffing and lead encephalopathy. Can Med Assoc J 1982;127:1195-1197.
41. Brady WJ, Stremski E, Eljaiek M, et al. Freon inhalation abuse presenting with ventricular fibrillation. Am J Emerg Med 1994;12:533-536.
42. Horowitz BZ. Carboxyhemoglobinemia caused by inhalation of methylene chloride. Am J Emerg Med 1986;4:48-51.
43. Stewart RD, Hake CL. Paint-remover hazard. JAMA 1976;235:398-401.
44. Machabert R, Testud F, Descotes J. Methaemoglobinaemia due to amyl nitrite inhalation: A case report. Hum Exp Toxicol 1994;13:313-314.
45. Bradberry SM, Whittington RM, Parry DA, et al. Fatal methemoglobinemia due to inhalation of isobutyl nitrite. J Toxicol Clin Toxicol 1994;32:179-184.
46. Bogart L, Bonsignore J, Carvalho A. Massive hemolysis following inhalation of volatile nitrites. Am J Hematol 1986;22:327-329.
47. Newell GR, Mansell PW, Spitz MR, et al. Volatile nitrites: Use and adverse effects related to the current epidemic of the acquired immune deficiency syndrome. Am J Med 1985;78:811-816.
48. Soderburg LS, Flick JT, Barnett JB. Acute inhalation exposure to isobutyl nitrite causes nonspecific blood cell destruction. Exp Hematol 1996;24:592-596.
49. Dax EM, Adler WH, Nagel JE et al. Amyl nitrite alters human in vitro immune function. Immunopharmacol Immunotoxicol 1991;13:577-587.
50. Meredith TJ, Ruprah M, Liddle A, et al. Diagnosis and treatment of acute poisoning with volatile substances. Hum Toxicol 1989;8:277-286.
51. Flanagan RJ, Ives RJ. Volatile substance abuse. Bull Narc 1994;46:49-78.
52. Katz RL, Bigger JT. Cardiac arrhythmias during anesthesia and operation. Anesthesiology 1970;33:193-213.
53. Scerri GV, Regan PJ, Ratcliffe RJ, et al. Burns following cigarette lighter fluid abuse. Burns 1992;18:329-331.
54. McGill-Rizer B. The 38-cent high. J Michigan Pharmacist 1994;32:138.
Physician CME Questions
65. Distal renal tubular acidosis is most commonly associated with which of the following substances?
B. Methylene chloride
66. The practice of inhaling solvent vapors after pouring them over a piece of cloth is called:
67. Which of the following statements regarding methylene chloride is true?
A. Delayed production of carbon monoxide may contribute to toxicity.
B. It is a common ingredient of typewriter correction fluid.
C. Its use is epidemiologically linked to Kaposi’s sarcoma.
D. Its use is more common among Native Americans.
68. Which of the following may be indicated in the treatment of amyl nitrite toxicity?
A. Cimetidine (Tagamet)
B. Dimercaprol (BAL)
C. Methylene blue
D. N-acetylcysteine (Mucomyst)
69. Which of the following may be seen with long-term solvent abuse?
A. Cerebral infarction
B. Paranoid psychosis
D. Peripheral neuropathy
70. Which of the following statements is true?
A. Although VSA has been linked to marijuana use, there is no association between VSA and IV drug abuse.
B. Inhalant use begins in grades 10-12 and increases steadily until graduation from high school.
C. The majority of VSA deaths occur from abuse of "whippets."
D. VSA is most commonly practiced in groups of adolescents.
71. Which of the following solvents is matched correctly with its source?
A. cigarette lightertoluene
B. fire extinguishermethylene chloride
C. paint stripperbromochromodifluoromethane
D. typewriter correction fluidtrichloroethane
72. Which of the following may be appropriate in the management of an adolescent who has been inhaling gold spray paint?
A. Furosemide (Lasix)
B. Hyperbaric oxygen
D. N-acetylcysteine (Mucomyst)
E. Oxygen therapy and inhaled beta-agonists